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For the paternal parent DM5, 351 (16.3%) of the 2154 mapped markers were distorted (P < 0.001), and two clusters of distorted markers were observed on LG 1D and 6B.
The assessment of marker transmission ratio distortion found that 26% of the genotyped markers were distorted from either 1 1 or 3 1 ratios expected for segregation of single dose markers in one or both parents, respectively.
A total of 18 markers were distorted in both F2 populations (Additional file 2: Table S2), and were thus caused by nuclear genetic factors.
In this study, 17.9% of mapped markers were distorted.
All 21 markers were distorted in favour of alleles from the wild female parent and 14 of these were found on linkage groups 4, 6, 8 and 11.
In total, 12 markers were distorted on chromosome 1D, 24 markers on chromosome 2D, 6 markers on chromosome 4D, and 10 markers on chromosome 5D.
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Conversely, a cytoplasmic effect can be inferred if the markers are distorted in only one of the reciprocal F2 populations.
Markers that were distorted significantly with P < 0.0001 were not considered because ratios that are too skewed might create inaccurate distances and false linkages (Cervera et al. 2001).
In the MMF2 map, 5.3% of the marker loci were distorted, ranging from 0.0% for Chr05 and Chr08, to 17.0% for Chr09 (Table 3).
We found that 26% of the genotyped markers were affected by TRD; however, only 17% of the markers included in the final maps were distorted.
The utility of this combination is further supported by the low observed frequency of SD, in which only seven (5%) of the 140 sequence-tagged site STS markers (0% after corrected-Bonferroni) were distorted (Table 2).
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markers were shared
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